H. pylori is a bacterium usually found in the stomach and the duodenum. Epidemiological studies confirm that H. pylori mainly spreads via contaminated water and foods. The prevalence of H. pylori infections among persons aged below 20% in underdeveloped countries and developing countries is as high as 80-90%.
Once a human being is infected with H. pylori, H. pylori ends up in the epithelium of the stomach. H. pylori produces urease which turns a tiny amount of urea existing in the stomach into alkaline ammonia to maintain the neutral environment at the site of H. pylori infection, thereby preventing H. pylori from being destroyed by gastric acid. Toxins and toxic enzymes produced by H. pylori are not only conducive to transfer and reproduction of H. pylori but also conducive to survival of H. pylori. 
H. pylori penetrates the mucosal lining of the stomach and thus reaches the neutral environment of the surface of the epithelium of the stomach, thereby damaging the epithelium of the stomach. During the aforesaid process, the epithelium of the stomach releases oxygen free radicals and protease products. The oxygen free radicals and protease products manifest toxicity on the epithelium of the stomach, causing chronic inflammations and digestive tract ulcers (i.e., open sores that develop on the inside lining of the stomach and duodenum). When not treated properly, the digestive tract ulcers may lead to complications, such as digestive tract bleeding, perforations, and gastric outlet obstruction, or even cause stomach cancer.
At present, the standard first-line therapy for H. pylori infection is triple therapy and quadruple therapy. At present, antibiotics for inhibiting H. pylori include clarithromycin, levofloxacin, metronidazole, tetracycline and amoxicillin. However, at present, the efficacy of the aforesaid therapies is low as a result of poor patient compliance, because of a lengthy therapeutic course for eradication of H. pylori, an overly large number (i.e., 10) of capsules to take each time, and side-effects of the aforesaid drugs for treating H. pylori infection include dizziness, diarrhea, furry tongue, insensitive to taste, and allergy.
Taiwan patent 1510255 discloses nanoparticles comprising crosslinked glucosamine and amoxicillin, wherein water-in-oil emulsion is formed by the introduction of anionic surfactants and oil, so as to crosslink glucosamine and encapsulate amoxicillin. The nanoparticles have an average particle diameter of 100 to 600 nm, the amoxicillin thus encapsulated accounts for at least 5% (w/w) of the total weight of the nanoparticles. When taken orally, the nanoparticles have longer retention duration in the stomach than free amoxicillin or microscale beads.
Taiwan patent 201138788 discloses a drug structure for treating digestive tract ulcers. The drug structure is formed by encapsulating a drug in algin functioning as a substrate to form a microsphere and then encapsulating the microsphere in a chitosan sheath. According to Taiwan patent 201138788 (the specification, page 7, lines 18-25), the drug structure is slowly released, by forming colloidal algin.
U.S. Pat. No. 6,284,745 discloses a drug structure which requires joint use of algin and chitosan. In the course of making the drug structure, calcium pantothenate is introduced so that sodium alginate for use in making algin forms colloidal beads to make a drug. The drug structure is capable of releasing an included drug instantaneously within two hours.
Taiwan patent 1482632 discloses polymerizing alginate and chitosan to form a drug carrier for use in eradicating H. pylori, releasing a drug effectively from the drug carrier in the gastric mucosa environment (pH 7.4) to inhibit the growth of H. pylori by the increase of interaction of alginate and chitosan molecules, and allowing the drug carrier to adhere to the gastric mucosa by means of mucoadsive of chitosan to thereby extend the duration of retention of the drug in the gastric mucosa.
The aforesaid patents disclose microsphere drug carriers or microsphere drug structures for inhibiting H. pylori. However, unsolved issues include: how to enhance therapeutic efficacy of a drug carrier or a drug structure so as to reduce the dosage of a drug to take each time and lessen the side-effects of the drug.